Wednesday, May 14, 2008

When is a high fat diet not a high fat diet? Stuff via Fanatic Cook

Here's an interesting paper brought my way by Dave Lull who browses Fanatic Cook, a place I'm not likely to visit in my travels. Though perhaps I should, to keep an eye on what the carbophiliac people are up to...

This paper is another in which a Western/Cafeteria diet (45% fat, 40% carbs) is described as high in fat and, wait for it, low in carbohydrate. Assuming 2400kcal per day, that's 1000kcal of carbs or 250g/d. You can appreciate the level of intellectual honesty here, so of course the temptation is to bin the paper. No, WAIT.

There's some interesting stuff. Never mind the shifts in cholesterol levels (it was a cross over study with a low-fat high-carb period), these are exactly what you would expect. The study was careful not to check the LDL particle sizes and numbers otherwise they might have found the small dense LDL which would probably have predominated on the HC period. That is along side the lower HDL figure they did report on the HC phase. They were also careful not to look at glycosylation levels (HbA1c would be useless in a short study like this, but fructosamine looks at two weeks of glycosylation and would have been interesting) to see what was happening in the "eating" world, rather than during a glucose tolerance test. You don't put this sort of control in to nutrition studies because it might not get you the answers you want. High fat diets DO tend to produce higher fasting glucose levels and can even produce higher fasting insulin levels, as here, but 24h AUC for insulin and glucose would be lower. Fructosamine would have shown this. That's how come I can sit here with an HbA1c of 4.4% and a fasting glucose of 5.5mmol/l, higher some days. No suggestion anywhere that Vidon et al or Fanatic Cook see things this way. I do. Shrug.

So, not my type of study. But look at this, this is what grabbed me:

"Lower cholesterol concentrations occurred despite a higher cholesterol synthesis rate (P less than 0.05) and higher HMG-CoA reductase mRNA concentrations (P less than 0.05). LDL receptor mRNA concentrations were unchanged, LRP mRNA concentrations were lower (P less than 0.01)"

The molecular techniques are a bit beyond me to comment on, so I'm just going to believe Vidon et al, that cholesterol synthesis went UP on the high carbohydrate phase diet, plasma levels went DOWN and gene expression for the LRP went DOWN.

Now, they were looking at HMG-CoA reductase in white blood cells, not the liver, but they seem to think the same thing happens in both places:

"Because synthesis and secretion in the plasma pool increased, it appears that the lower plasma cholesterol concentrations were related to increased removal from plasma. However, the mRNA concentrations of 2 main lipoprotein receptors that control the clearance of cholesterol from plasma were unchanged (LDL receptors) or decreased (LRP)"

Now I find this very interesting. More cholesterol produced, less is taken up, yet plasma level drops.

Here's an ad hoc hypothesis as good as anything in the paper:

Some receptor other than the LDLr or the LRP is taking up the LDL cholesterol.

Lets have a guess at which one, let's guess at the oxidised cholesterol receptor. There is at least one short term intervention study showing that small reductions in total fat calories in the diet increase the level of oxidised LDL in the blood, markedly. There was a 15% difference in the fat content of the two diets in Vidon's study. Oxidised LDL is eaten by macrophages, using the oxLDL receptor. They become foam cells in fatty streaks.

Perhaps the cholesterol levels drop as it's all now in foam cells on the arterial walls????

Never forget the American paradox. According the Vidon et al there must a sharp reversal of those benefits associated with increasing fat from 18% of calories through to 32% (p less than 0.001 for trend by quartiles) if you extend it to 45%. Duh.

Maybe, maybe not.



donny said...

In the post before that one, Fanatic Cook writes about an Insulin Index study where beef caused a higher rise than noodles, and fish a higher rise than microwave popcorn.
The lowest insulin response in that study was to peanuts. (around 72 percent fat) The next lowest response was to eggs (66 percent fat.) So the study used by this person to show that high protein causes hyperinsulinemia 1) doesn't and 2) sort of refutes the study in the second post claiming that high fat causes hyperinsulinemia.

donny said...

Whoops. That was Beef and Oatmeal. Cheese goes with noodles.

Peter said...

Hi Donny,

Dave pointed me at that post too,these were my thoughts about it to him:

From the beef paper:

"When possible, foods were presented under a large opaque plastic hood with a hole through which volunteers pulled out pieces of the test food one at a time. This was an attempt to minimize between-subject variation in cephalic phase insulin secretion arising from the sensory stimulation
associated with the anticipation and act of eating (27)."

Ref 27 cannot be easily followed so try this one.

Beef tastes much better than porridge, plus various amino acids are insulogenic, certainly those in casein, probably in beef too. The body compensates for this with glucagon. NB I wouldn't eat a high beef diet anyway, 60-70g protein per day total is my normal intake. Folks on Dr Bernsteins diabetes forum usually report that oatmeal mangles their blood glucose levels. Beef doesn't. I would trust this source more than the Aussie paper. You can choose, Fanatic Cook has no choice, being a non beef eater!

Back to talking now:

I have trouble giving credence to any of the Fanatic Cook posts Dave has pointed me towards. Her thinking seems very shallow, in terms of analysis and thinking beyond berries and wholegrains being good for us and meat is carcinogenic. No thanks.


carrmh37 said...
Karen E. Foster-Schubert, Joost Overduin, Catherine E. Prudom, Jianhua Liu, Holly S. Callahan, Bruce D. Gaylinn, Michael O. Thorner, and David E. Cummings
Acyl and Total Ghrelin Are Suppressed Strongly by Ingested Proteins, Weakly by Lipids, and Biphasically by Carbohydrates
J. Clin. Endocrinol. Metab., May 2008; 93: 1971 - 1979.
I thought this paper was interesting. The authors manuscript is free. the prolonged effects of protein on insulin the acute effects of lipid on triglycerides and the effects of glucose on ghrelin would encourage me to eat amixed diet but perhaps not too much of anything. How you achieve the not too much is probably the cause of the disagreements between advocates of different diets.

Peter said...

Hi carrmh37,

I keep hitting a request for payment for access that doesn't have an athens account option, so I can't get the full text.

Just from the abstract, where only the ghrelin effects are reported, I can't see much to make me want to eat carbohydrate as a source of bulk calories. Protein would be fine if more of an orexigenic effect was needed than provided by fat, but at the cost of an insulin spike.

What makes you feel differently? Bear in mind that they are looking at a single liquid shake of (to me) unknown composition except the protein/carb/fat label, done once for each participant, in each section of the crossover study, presumably on to a SAD background...


Peter said...

sorry, typo, should have been anorectic effect


Chainey said...

Re. "Intellectual honesty": That's important to me too--perhaps the most important thing, but keep in mind that it depends on one's underlying assumptions how one interprets data. Forty-five percent fat probably sounds "high" to most people, so they might be misguided rather than dishonest.

carrmh37 said...

Hit 'authors manuscript pdf' instead of pdf. They measured insulin, glucose and triglycerides for 6 hours after the test meal

Peter said...

Hi carrmh37,

The biochemistry shows that a sugar drink, a protein shake and a fat drink all behave exactly as you would expect, bearing in mind that only 80% of calories were in the form of the named macronutrient. So the fat drink spiked insulin because it was, err, 10% carbohydrate. The insulin spike managed this carbohydrate dose without hyperglycaemia, good old first phase insulin response, that's why we have it!

The trigs peaked at 3h after the fat drink. It's a fat drink. You can't drink fat without making chylomicrons or else you develop steatorrhoea, give me the chylomicrons any day. Did you notice the NS dip in trigs in the carbohydrate line? This began just after insulin peaked and was trending back upwards by 6h. All NS trends, but these people have just stored 100g of carbs under peak insulin effect. They might be stored as a glycogen load, they might be the beginnings of fatty liver and get shunted out of the liver later as VLDL triglycerides. VLDL and chylomicrons are very different. They come up the same on lab tests.

I noticed that there was no statistically significant difference between protein and fat drinks at any time point for the acetylated ghrelin curves. How does generate the idea that protein is more satiating than fat, with nothing to be seen on the VAS scores for appetite? Obviously both lipid and protein were different from carbs between 3h and 6h, but not from each other...

So I can't see where the conclusion of the paper comes from (protein for weight loss, fat for weight gain), surely their data suggest that by three hours people are going to be hungry after carbs (based on ghrelin rather than VAS for hunger) and this is an ideal time for another carb snack if you want weight gain at the cost of hyperinsulinaemia? Then another 3h later, another at midnight and 3am and.......

That just leaves me with wondering why you feel, from this specific paper, that eating a little of everything in moderation might be a valid approach? What am I missing? It suggests to me that to eat adequate protein (as we all must), control appetite with fat and expect to be hungry 3h after carbs is probably how metabolism would work well...

Anyway thanks for the paper, the biphasic response to ghrelin is interesting!


JohnN said...

It's misleading to just talk about peak insulin; total insulin production per meal (insulin integrated over time) is better.
I would look at the first phase insulin response as a fixed overhead cost. Example: consider a dinner where a meat course (protein and fat) is followed by a cheese course (casein and fat) and then ice cream (or chocolat cream pudding) for dessert - more casein and some sugar - there will be only one initial spike of insulin when the meal is anticipated by the brain (first phase response); total insulin per unit calorie is still rather low. As a matter of fact, total insulin should be proportional to the amount of glucose converted by the liver from the meal modified by your own level of insulin sensitivity.
Does that make sense?

Stephan said...

I'd just like to point out that it's not necessary to avoid insulin spikes or even large amount of glucose flux through the blood (as long as the blood glucose concentration doesn't go too high).

The Kitavans showed us that. 70% calories from "paleo" carbs, no hyperinsulinemia or hyperleptinemia. No hypertension, CVD or overweight. The same is true of other cultures in the pacific islands, S America and Africa.

What do they have in common? They typically don't eat grains, and they process seeds by soaking or fermentation.

Anonymous said...

From the American Paradox:
"a higher saturated fat intake was associated with a smaller decline in mean minimal coronary diameter.. and less progression of coronary stenosis...
"Carbohydrate intake was positively associated with atherosclerotic progression.. particularly when the glycemic index was high.
"Polyunsaturated fat intake was positively associated with progression when replacing other fats...but not when replacing carbohydrate or protein.
"Monounsaturated and total fat intakes were not associated with progression."

Conclusion: the ideal diet would be high in total fats, saturated fatty acids, and MUFAs, lower in protein, PUFA, and carbs. Seems like they're on the same page as Jan Kwasniewski and Peter, eh?

Anonymous said...

I think raw carbohydrates will also have a different effect. Comb honey can't be compared to table sugar if you want to maintain some semblance of intellectual honesty. What makes the Kitavans different from British and Americans? They eat real foods, unprocessed, free of additives, and very fresh. They don't eat a lot of PUFA oil, refined sugar, flour, and hydrogenated oils. Of course, given time, they probably will convert to the same unhealthy Western Diet - a steady stream of white flour, HFCS, sugar, Crisco, and soybean oil. The stuff that weak and diseased bodies around the world are made of.

Charles R. said...

RE: Porridge

I am a paleo eater, or as much as I can be. My diet is generally at least 65-75% fat, calorie-wise. Sometimes higher.

But I gotta say that I can eat my eggs and pemmican in the morning, and be hungry a couple of hours later. But if I eat a bowl of oatmeal, usually with butter, but not always, I really am not at all hungry until mid-afternoon.

This is my own little paradox that I have never been able to understand. But the effect has been consistent over a number of years. It makes me angry, because I can't figure it out, but it's a real phenomenon.

I probably should get a blood sugar monitor and watch what happens over time...

Paul said...

Charles -

A blood sugar monitor only costs about $20 so it's worth doing. The cost comes in the test strips (about $1 each) but if you are just doing occasional checking, that's obviously not a big issue.

I have a small or sometimes non-existent rise in blood sugar one hour after eating, a peak at two hours, and a return to a lower number at three hours. That's quite different to what is described as normal response (return to normal after two hours). I wondered if other low-carb high-fat eaters had seen anything similar?

Stephan -

You mentioned the Kitavans as high-carb and healthy. Isn't the same true of traditional Japanese diet (from the point of view of longevity)? I cannot track down percentage of calories from carbohydrate in such a diet, so I may be on the wrong track,


Anna said...

Just an aside about Bix's blog, The Fanatic Cook. Last fall, around the time she started really amping up her fanaticism with reducing animal protein and fat and raising cold resistant starch (following what she described "cancer scares" with herself and family members), she started comment moderation and then emailed me to say she wasn't posting my comments anymore. She's a nutrition professional working with diabetic clients, so I guess she took personally my comments posted *on another blog* about diet & nutrition authorities having a lot to answer for with their advice of the past few decades, especially for diabetics.

Later, two other other commenters in email exchanges with me (which similar views and somewhat similar experiences with BG to mine) noted that she was not longer posting their comments, either (both always made cordial comments, but often voiced views that conflicted with what Bix thinks the evidence says). But she didn't email those folks to say they were blacklisted, like she did with me. Either way, she is now appearing to be very selective about which comment she posts and which she doesn't.

It's her blog, and she certainly can call the shots regarding comments on her blog. But I find it interesting that she is so threatened by those that don't share her view that she censors their views. I noted the commenting in general changed quite a bit there from that point on, from a tone of interesting, thoughtful discussion, to a tone like a " Bix fan club".

Luckily, I found more interesting blogs to read :-).

Anna said...

I never really know what to think about glucose and insulin studies that don't use subjects who are pre-diabetic, like me. I'm pretty sure my first phase insulin response is shot. Second stage is still robust, but can result in a unpleasant BG low, so I avoid foods that instigate it very much. So many of the studies use subjects with healthy glucose regulatory systems, or they use subjects with full-blown diabetes. There don't seem to be as many good studies with those of us in between.

Then again, I doubt I'd participate in such a study, unless it was really short term, exercise-based, or I could report what I was am already doing, because I can't risk messing with the degree of BG control I get already with diet, on my own. I'd drop out of any study that had me eating long term in a way that I already know is damaging.

team smith said...

charles r., i have the same problem as you--an hour after eating what i feel is a high fat and moderate protein meal i am really hungry. i thought i solved it a while back when i actually felt "starving" all the time and i upped my fat such as coconut oil significantly. but these days the only meal i feel lasts me the whole morning is my 1/2 c. milk, 1 c. cream and 8 raw egg yolks in a shake. even when i put 4 tablespoons of butter in a small potato to have with my meat it never seems enough.

what would checking my glucose tell me? i mean, what would i need to change? paul, you say it's not a bad idea to get a glucose monitor and check it every once in a while--how would i know what i am looking for?

thank you...amanda

Peter said...

Hi JohnN,

Looks to me as if cephalic phase precedes first phase, probably both are relatively fixed overheads... Yes, after that insulin production should be proportional to digested/produced glucose and modified by insulin sensitivity. The one peculiarity seems to be insulogenic amino acids which need glucagon to compensate. Whether these are also gluconeogenesis substrate amino acids I've not checked...


Peter said...


Still not had time to start on the insulin signaling paper you shared. Obviously avoiding hyperglycaemia side steps a host of problems. So, with good insulin sensitivity, does "appropriate" insulin do any harm on the insulin/longevity aspects?


Peter said...

Hi Charles and Paul,

Flicking through ItsTheWoo's comments on the second main diazoxide post it's pretty clear that there are a lot of aspects to hunger. I'd agree a blood glucose meter is useful, if you have physiological insulin resistance from a high fat diet and drop a glucose load on it you might end up quite hyperglycaemic for some time. My rule of thumb is never above 140mg/dl and 100mg/dl more acceptable post prandially. My morning FBG is always higher than through the rest of the day, the dawn phenomenon. There are a few interesting papers around on this latter aspect.


Paul said...


About what to check -

fasting blood glucose preferably in the 80s, or in the 90s (Peter has commented more than once that the Kwasniewski type diet can give high-ish fasting blood glucose, but I'm still unclear about that)

post-prandial blood glucose not heading into the danger zone above 140

If either of those were high, it would tell you to reduce carbohydrates. It also might help you identify if specific foods were responsible for jumping your blood glucose levels.

I would say the price and ease of use make a blood glucose meter pretty much like a thermometer, an item you might as well have. Roll on more home blood tests and less need for doctors...


Peter said...


Having read a few of Bix's posts, nothing you say surprises me. But it's what people want to hear, or have been convinced they want to hear anyway...


Paul said...

(Peter - thanks, I mailed about BG just as your own reply about BG was posted, Paul).

Peter said...

Ha, beat you to it Paul (just!).

Amanda, if you get as far as doing an OGTT don't forget to carb load for three days, 150g/d or you'll come out diabetic. Also always wash and dry your hands pre finger sticking. Glucose gets everywhere, especially of you are carb loading or have just drunk 75g of glucose powder in water. The machine picks it up on your fingers. They're also notoriously inaccurate. Dr Bernstein's site will tell which he currently recommends. He knows better than anyone else.


Anonymous said...

It's also interesting to note that the "high fat (and high-carb) diet" had 15% PUFAs, while the lower-fat and higher-carb diet had 10% PUFAs. So maybe that explains the study's observations. Both had equal ratios of SFAs, MUFAs, and PUFAs, quite a strange diet. Both had 2 or 3 times more PUFAs than humans require. So there is no way to isolate whether the effect was caused by total fat, SFAs, MUFAs, PUFAs, or carbs. More garbage from a third-rate blog that hypes the high-fiber, low-protein, low-fat, complex-carb diet.

They say most of the saturated fats came from butter, cheese, and meat, but don't say where the other fats came from. Maybe processed oils and salad dressings and mayonnaise. The study also doesn't say what sources were used for carbohydrates, except that they had the "same proportions of simple and complex" carbs in the "high-fat" and "high-carb" diets.

The "high-fat" dieters also ate 10% more calories - which could account for the changes. But they ignore it and blame the fats instead. Another study defying the scientific method and failing to isolate variables.

Charles R. said...

"physiological insulin resistance from a high fat diet"

That's interesting. I vaguely remember seeing something about that, but can someone elaborate?

So I'm starting to think that it's the high protein aspect of the breakfast that results in hunger. I'll dump the egg whites, reduce the protein and see what effect that has.

Thanks, all, by the way, for the interesting discussion.

Peter said...

Hi Charles,

I stuck my thoughts down here about physiological insulin resistance. Apart from iwilsmar on Dr Bernstein's forum the other person I've seen on the net with this phenomenon is Jenny Ruhl of Blood Sugar 101. Oh, and now Bix too. None seems to regard it as an normal feature of a high fat diet. Dr B also doesn't, he aims for ALL BG readings to be 83mg/dl. But he's dealing with full blown diabetics and will start with metformin and work up from there to avoid this. I'm out on a limb here (again). A nightly shot of alcohol often works to drop morning blood glucose too.

Need another post on this but now my son's down with chickenpox and so, because nursery is out, there won't be a lot of time (not that there ever is!).


Anna said...

Just a reminder for those who casually use glucose meter test strips - once the vial of strips is opened, it must be used relatively quickly, as the strips can go "stale" even if not subjected to temp and humidity extremes, etc. "Stale" strips will appear to work properly, but can give inaccurate results. Check your label for the maximum recommended time frame after opening and use opened strips before then.

I go through phases of testing frequently and testing only sporadically, so I always date my vial when I open it for the first time.

Charles R. said...


Thanks for that link! I remembered reading about that issue somewhere, but couldn't remember where.

As one commenter said on that post, it was great, and I have a much-changed perspective on the subject now. For the life of me, I couldn't figure out why I had a FBG of 101, given my diet. Now I understand. And per Sasquatch's and your comments, I know why that (very unusual) baked potato and N/A beer the other night really through me for a loop...

Paul said...
This comment has been removed by the author.
Stephan said...


I can't tell from the paper. There's so little in common between the long-lived lines it's hard to draw any conclusions. Some lines are more insulin-sensitive, some are more insulin-resistant. The insulin-sensitive mice have lower fasting insulin, resistant mice have higher insulin. I'm not sure if that tells us anything. Plasma glucose seems to be down in all the lines they've looked for it. You'd probably be able to get more detailed info from the primary sources but I'm not feeling motivated enough to go through them all.


The traditional Japanese diet is high-carb as far as I know. I'm not sure I'd place it on the same level as the Kitavan diet though. Japanese on a traditional diet have a short stature (probably due to mineral deficiency from the phytic acid in the rice), low muscle mass and a high risk of stroke. They are far healthier than Americans though.

Stephan said...

Oh and by the way Peter, I'm always a little skeptical of the aging studies because are they really looking at fundamental aging processes or just resistance to processed mouse chow-induced disease?

I know that mice kept under regular lab conditions die of tumors and other nasty things much earlier than if they're kept in an enriched environment with exercise and better food. I think genetically wild mice also live longer than inbred strains even if raised under lab conditions.

So it's hard to know exactly what these studies are telling us.

Paul said...


Your comments about stature of Japanese people and American health isn't connected with this, but it reminded me of this story from last year


"Americans, who have been the tallest in the world for a very long time, are no longer the tallest," said John Komlos of the University of Munich, who has published a series of papers documenting the trend. "Americans have not kept up with western European populations."

There's an intriguing statement

Komlos and others have shown that growth of the average American flagged beginning in the 1950s, allowing other countries to overtake the United States by the 1970s.

which suggests it might be possible to tie change in stature to something specific that changed in the US compared to the rest of the world back then. If you do a whole lot of very careful research that is...


Anonymous said...

Stephan: "I'm always a little skeptical of the aging studies because are they really looking at fundamental aging processes or just resistance to processed mouse chow-induced disease?"

I'm skeptical of most studies, just for that reason alone. If they feed animals a diet consisting of casein powder, refined sugar, white flour, and PUFA oils, of course they would die sooner of some disease and live longer when some aspect of the diet was restricted (protein, fat, carbs or calories). Most of these studies just tell me us that the scientists who conduct them are all fools, and know nothing about nutrition. There is no way to build a synthetic diet that is as good as natural foods.

Anonymous said...

"Amanda, if you get as far as doing an OGTT don't forget to carb load for three days, 150g/d or you'll come out diabetic."

That's interesting because when the Eskimos were tested on their native diet, they had normal OGTT.

"Heinbecker studied the tolerance of Eskimos to carbohydrate. His subjects, by necessity, lived on a practically exclusive meat diet for years, before their carbohydrate tolerance tests were made. In spite of the fact that their diets were low in carbohydrate, the results of the tests indicated that they assimilated carbohydrate
well. The blood sugar curves were within the normal range and the urine remained free of sugar."

Any theories on why the Eskimos did not have problems handling glucose, but Stefansson and his partner did? The study speculated that they were protected by eating more protein or carbohydrate than Stefansson did on his meat diet. Maybe they were more active. But something in their diet kept their glucose response normal, even on a carnivorous diet.

Peter said...

Stefansson reported the ketosis in the Eskimo was always mild, so probably more protein. No suggestion of even moderate carb intake in any of his books. Possibly their omega 3 fat intake normalised their insulin responsiveness.


Anonymous said...

They got carbs from meat. The study said 53 grams a day, in the Eskimos studied, eating totally carnivorous diet. They did eat berries in small amounts, but these were only picked one season of the year, and used in small amounts. Stefansson ate a lot less protein and carbs since he ate less variety than them probably.

Peter said...

I've a norwegian paper in norwegian that has the Greenland Eskimo eating 150g of protein (fish/seal) per day. Must be a fair dose of glycogen in that too... No biochemistry included and I can only just make out the tables of macronutrient intake, the text is a foreign language to me.


Anna said...

My lab and doctor do not inform to eat 150 gms of CHO per day for 3 days prior to, so when I called the lab to ask about it last year prior to my most recent GTT, I was told it wasn't necessary (when I flunked the 1 hr and 3 hr GTT ten years ago, I know I had lots o' carbs prior to the tests - I don't even want to say what I remembering having instead of dinner the night before the 1 hr GTT that started my glucose journey). I really didn't want to subject myself to that many CHOs for that long, now that I know how high that many CHO gms send my BG.

According to Jenny at (formerly known as What They Don't Tell You ABout Diabetes), the difference is only about 10 mg/dl more for any post-meal result that is over 140 mg/dl at 2 hours, if you are currently low carbing (rough estimate).

Peter said...

Hi Anna,

I too was unwilling to carb load, but by the time my FBG had drifted up to 5.5mmol/l on fairly stringent LC I wanted to know if I was a genuine prediabetic. The carb loading dropped my FBG to 4.3mmol/l by the third day. Yams, sweet potatoes and bananas. Never got above 7.0mmol/l during the carb load. The two hour OGTT value was 3.4mmol/l, reactive hypoglycaemia. Doesn't surprise me as I've always done this as far as I can remembe. If I would hit the simple carbs at 3pm I'd be wobbly by 5pm and needed to snack in the middle of evening consults. A few bikkies did the job until 7pm. Then another few before heading home. We had lots of boxes of biscuits in the practice. The nurses used to hide the best ones from me!

Of course, as Jenny is emphatic, there is no reason why carb restriction and normal bodyweight should stop type 2 diabetes. If it's plasticisers in the food chain which cause it, you can eat what you like 'til it gets you (maybe avoid plastic), then eat to your meter thereafter. Maybe she's correct. Maybe not...

So my real question would be what would happen to someone who's 2h OGTT was going to be 3.4mmol/l with carb loading. Would the lack of carb load only shift it to 3.7mmol/l, or might it hit 8.0mmol/l?

How much to I want to know? (Peter thinks unpleasant thoughts about 75g of the glucose in the kitchen).


Anna said...

Hmmm, maybe I'll try a home GTT (using my meter, which compares pretty well with my lab results) with 3 days of prior carb loading one of these weekends when the "boys" are away camping, as a comparison. Wouldn't want to do it on a normal time, as roller coaster BGs from eating higher carbs really make me cranky these days, especially during the reactive lows.

Douglas Porter said...

isdgfbfoI think that one thing that is being missed in the comments about insulin and blood sugar is micronutrients and how they affect the basic regulatory mechanism. If you google diabetes along with various other terms like vitamin D, or chromium, or molybdium, or zinc, etc., you will find various papers correlating the two. It is not all macronutrient ratios. Vitamin D works at the nuclear level. The various elements work as cofactors in enzyme systems, just like Cobalt in the B12 molecule. If you have no cobalt, then there is no B12 molecule. This is the big difference between eating an unrefined diet and a refined diet, the loss of micronutrients. Katavians or Eskimos are eating an unprocessed diet with food from the sea or at least not from fields that have been cultivated for centuries and so that have a much better chance of getting the micronutrients they need. This is an area that gets very little study or attention. Even if you eat an unrefined diet, it is hit or miss if you get them. It just all depends on the area you are in, though by the ocean you will get them all. E.g. Iodine shortage is huge in much of the world and therefore endemic goiter is very common. There was a research dentist from Loma Linda University, Ralph Steinman, who did a number of mostly rat experiments showing how dentinal fluid transport (which is the fluid flow through the tubules of the teeth from the pulp to the exterior)reversed under various conditions of carb loading, and how it could be corrected with micronutrients, from unrefined food. As Itsthewoo says elsewhere, one thing is the basic mechanism, and the second is what you do when it gets broke (restrict carbs)


Douglas Porter said...

About Bernstein and fasting BG levels. Bernstein wants them down and he will get them down using insulin if that is what it takes. You could do the same thing if you wanted. Just use slow acting insulin at night like Bernstein would do. The decision on what is optimum blood sugar over the course of the day and how you get there is really at some point is a personal or aesthetic one. Read William Jefferies on the Safe Uses of Cortisol, where he supplements a hormone on otherwise healthy people who have health challeges or think about older people who take sex hormones for depleted levels for improved feeling of wellbeing even though they are clinically not diagnosed with any disease.


Anonymous said...

Peter and Anna, I don't think there is any need to carb-load. Instead I would suggest eating a high-protein diet before the test. Say 2# (1 kg) of meat, whole eggs instead of just yolks, and so forth. Reduce the fat and increase protein slightly and I bet the tests won't say that you're diabetic any more. Why add carbs if protein will do the same thing?

Anonymous said...

Douglas Porter: "This is the big difference between eating an unrefined diet and a refined diet, the loss of micronutrients... Even if you eat an unrefined diet, it is hit or miss if you get them."

I have made this point, frequently. Most animal studies use a worthless diet of refined sugar, corn starch, casein, and high-PUFA oils (usually corn oil or something like that). A lot of people eat similar diets, so of they're obese, diabetic, glucose intolerant, etc. Also, as you point out, simply eating "unrefined food" (carbs) won't always work. There is also the issue of bio-availability, and how much nutrients are required for the body to process a food. Fat seems to require less nutrients for digestion and assimilation, calorie for calorie, than carbs or protein. This explains the success of people like Jan Kwasniewski.

I am very skeptical of studies that use "foods" like refined grains and sugars, purified proteins, and high PUFA vegetable oils. Even using say lard is misleading, unless you also feed another group beef fat or foie gras as a control. Lard has about 4 times more PUFAs than beef, so lard might cause problems that beef suet would not cause. So, a study should compare like a dozen fats, covering a wide spectrum of types.

There is also a tendency for people in the low-carb world to assume all carbs are bad, based on studies for refined carbs and/or grains, and it is obviously invalid to extrapolate from refined food to unrefined. But that is what many people do. And it really bugs me, because it isn't in keeping with the scientific method. All variables should be isolated or the results are not science.

Peter said...

Hi Porter,

Yes, I guess exogenous insulin would do the trick, as would nightly alcohol or metformin. As my 24/7 average is low I'm happy as I am. A post on high fat mice is half written, elevated fasting glucose seems to be generic for high fat eating, certainly if the fat is primarily saturated. Not seen the effect mentioned in corn oil or fish oil studies.

Bruce, yes, I guess protein would stock up glycogen without sugar spikes. It was a bit strange in an interesting way to eat yams or sweet potatoes with three meals each day though... Loads of washing up too.

One of the benefits of the relatively low fat content of pork mince is that you can easily reinstate it with butter or dripping as you cook.

Eating food seems like a good idea.